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Main Title Influence of experimental pulmonary emphysema on toxicological effects from inhaled nitrogen dioxide and diesel exhaust /
Author Mauderly, J. L. ; Bice, D. E. ; Cheng, Y. S. ; Gillett, N. A. ; Henderson, R. F.
Other Authors
Author Title of a Work
Bice, David E.
Cheng, Yung S.
Gillett, Nancy A.
Henderson, Rogene F.
Pickrell, John A.
Wolff, Ronald K.
CORP Author Lovelace Biomedical and Environmental Research Inst., Albuquerque, NM. ;Harvard School of Public Health, Boston, MA.;Health Effects Inst., Cambridge, MA.
Publisher Health Effects Institute,
Year Published 1990
Report Number HEI/RR-89/30
Stock Number PB90-247347
Subjects Nitrogen dioxide--Physiological effect ; Respiratory organs--Diseases
Additional Subjects Nitrogen dioxide ; Diesel engines ; Exhaust emissions ; Toxicology ; Pulmonary emphysema ; Exposure ; Inhalation ; Rats ; Hyperplasia ; Lung ; Air pollution effects(Animals) ; Pulmonary alveoli ; Disease susceptibility
Library Call Number Additional Info Location Last
NTIS  PB90-247347 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 61 pages ; 28 cm.
The hypothesis tested in the project was that rats with preexisting experimentally-induced pulmonary emphysema were more susceptible than rats with normal lungs to the adverse effects of exposure to NO(sub 2) or diesel exhaust. Rats were exposed by inhalation seven hr/day, five day/wk, for 24 months to NO(sub 2) at 9.5 ppm, or to diesel exhaust at 3.5 mg soot/cu m, or to clean air. Pulmonary emphysema was induced in one-half of the rats by intratracheal instillation of elastase, six weeks before exposures. Nonneoplastic endpoints were evaluated after 12, 18, and 24 months of exposure. Nitrogen dioxide exposure of normal rats caused mild epithelial hyperplasia and inflammation in proximal alveoli. Significant interactions between the influences of emphysema and nitrogen dioxide were demonstrated to be additive for four parameters (out of 61 parameters). Diesel-exhaust exposure of normal rats caused progressive, focal inflammation, and epithelial proliferation. The final soot lung burden was only one-third of that in nonemphysematous lungs.
Cover title. "October 1989"--Page 4 of cover. Includes bibliographical references. "Includes commentary of Health Effects Review Committee." Microfiche.